ArticleeLife2016
The Drosophila HNF4 nuclear receptor promotes glucose-stimulated insulin secretion and mitochondrial function in adults.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 106 citations in OpenAlex.
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- Genomic and insulin-mediated control of metabolic homeostasis by the mosquito ecdysone-induced gene E93.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.PLoS biology · 2025Article
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- Presence of mitochondrial dysfunction in a case of Fanconi syndrome with normoglycemic MODY1.CEN case reports · 2025Article
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- TIFAB modulates metabolic pathways in KMT2A::MLLT3-induced AML through HNF4A.Blood advances · 2025Article
- 2,4-Dinitrophenol is toxic on a low caloric diet but extends lifespan of Drosophila melanogaster on nutrient-rich diets without an impact on metabolism.Biogerontology · 2024Article
- A nutrient responsive lipase mediates gut-brain communication to regulate insulin secretion in Drosophila.Nature communications · 2024Article
- Restricting bioenergetic efficiency enhances longevity and mitochondrial redox capacity in Drosophila melanogaster.Aging cell · 2024Article
- Two mitochondrial DNA polymorphisms modulate cardiolipin binding and lead to synthetic lethality.Nature communications · 2024Article
- Insulin signaling in development.Development (Cambridge, England) · 2023Article
- Time-series analysis of transcriptomic changes due to permethrin exposure reveals that Aedes aegypti undergoes detoxification metabolism over 24 h.Scientific reports · 2023Article
- The mitoepigenome responds to stress, suggesting novel mito-nuclear interactions in vertebrates.BMC genomics · 2023Article
- A bioinformatics screen reveals hox and chromatin remodeling factors at the Drosophila histone locus.BMC genomic data · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Although mutations in HNF4A were identified as the cause of Maturity Onset Diabetes of the Young 1 (MODY1) two decades ago, the mechanisms by which this nuclear receptor regulates glucose homeostasis remain unclear. Here we report that loss of Drosophila HNF4 recapitulates hallmark symptoms of MODY1, including adult-onset hyperglycemia, glucose intolerance and impaired glucose-stimulated insulin secretion (GSIS). These defects are linked to a role for dHNF4 in promoting mitochondrial function as well as the expression of Hex-C, a homolog of the MODY2 gene Glucokinase. dHNF4 is required in the fat body and insulin-producing cells to maintain glucose homeostasis by supporting a developmental switch toward oxidative phosphorylation and GSIS at the transition to adulthood. These findings establish an animal model for MODY1 and define a developmental reprogramming of metabolism to support the energetic needs of the mature animal.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.